Evidence map›Paper›PMID 26061814›Full record

ArticleOncotarget2015

p53 attenuates AKT signaling by modulating membrane phospholipid composition.

Natalia Rueda-Rincon, Katarzyna Bloch, Rita Derua, Rajesh Vyas, Amy Harms, Thomas Hankemeier, Niamat Ali Khan, Jonas Dehairs, Muralidhararao Bagadi, Maria Mercedes Binda and 3 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.0field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

33 citing papers in PubMed, 47 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 5 institutions in 2 countries.

Natalia Rueda-RinconKU Leuven - University of Leuven, Department of Oncology, Laboratory of Lipid Metabolism and Cancer, Leuven, Belgium.
Katarzyna BlochKU Leuven - University of Leuven, Department of Oncology, Laboratory of Lipid Metabolism and Cancer, Leuven, Belgium.
Rita DeruaKU Leuven - University of Leuven, Department of Cellular and Molecular Medicine, Laboratory of Protein Phosphorylation and Proteomics, Leuven, Belgium.
Rajesh VyasKU Leuven - University of Leuven, Center for the Biology of Disease, Laboratory for Molecular Cancer Biology, VIB, Leuven, Belgium.
Amy HarmsDivision of Analytical Biosciences, Leiden Academic Centre for Drug Research, Leiden University, The Netherlands.
Thomas HankemeierDivision of Analytical Biosciences, Leiden Academic Centre for Drug Research, Leiden University, The Netherlands.
Niamat Ali KhanKU Leuven - University of Leuven, Department of Oncology, Laboratory of Lipid Metabolism and Cancer, Leuven, Belgium.
Jonas DehairsKU Leuven - University of Leuven, Department of Oncology, Laboratory of Lipid Metabolism and Cancer, Leuven, Belgium.
Muralidhararao BagadiKU Leuven - University of Leuven, Department of Oncology, Laboratory of Lipid Metabolism and Cancer, Leuven, Belgium.
Maria Mercedes BindaInstitut de Recherche Expérimentale et Clinique (IREC), Pôle de Gynécologie, Bruxelles, Belgium.
Etienne WaelkensKU Leuven - University of Leuven, Department of Cellular and Molecular Medicine, Laboratory of Protein Phosphorylation and Proteomics, Leuven, Belgium.
Jean-Christophe MarineKU Leuven - University of Leuven, Center for the Biology of Disease, Laboratory for Molecular Cancer Biology, VIB, Leuven, Belgium.
Johannes V SwinnenKU Leuven - University of Leuven, Department of Oncology, Laboratory of Lipid Metabolism and Cancer, Leuven, Belgium.
KU Leuven · BECentre for Human Drug Research · NLDirectorate-General Joint Research Centre · BENetherlands Metabolomics Centre · NLVIB-KU Leuven Center for Cancer Biology · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The p53 tumor suppressor is the central component of a complex network of signaling pathways that protect organisms against the propagation of cells carrying oncogenic mutations. Here we report a previously unrecognized role of p53 in membrane phospholipids composition. By repressing the expression of stearoyl-CoA desaturase 1, SCD, the enzyme that converts saturated to mono-unsaturated fatty acids, p53 causes a shift in the content of phospholipids with mono-unsaturated acyl chains towards more saturated phospholipid species, particularly of the phosphatidylinositol headgroup class. This shift affects levels of phosphatidylinositol phosphates, attenuates the oncogenic AKT pathway, and contributes to the p53-mediated control of cell survival. These findings expand the p53 network to phospholipid metabolism and uncover a new molecular pathway connecting p53 to AKT signaling.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsCell Line, TumorCell SurvivalCyclin-Dependent Kinase Inhibitor p21Disease ProgressionFatty Acids, UnsaturatedGene Expression ProfilingHumansImidazolesLipidsMaleMiceMice, Inbred C57BLMice, TransgenicNeoplasmsAKT1 protein, humanCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21Fatty Acids, UnsaturatedImidazolesLipidsMDM2 protein, humannutlin 3PhospholipidsPiperazinesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-mdm2Stearoyl-CoA DesaturaseSterol Regulatory Element Binding Protein 1TP53 protein, humanTumor Suppressor Protein p53cancerp53phospholipidsSCDSREBP

Identifiers

PMID26061814
PMCPMC4673262
OpenAlexW1552458787

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.